Abstract
HIV infects several cell types in the body, including CD4+ T cells and macrophages. Here we review the role of macrophages in HIV infection and describe complex interactions between viral proteins and host defenses in these cells. Macrophages exist in many forms throughout the body, where they play numerous roles in healthy and diseased states. They express pattern-recognition receptors (PRRs) that bind viral, bacterial, fungal, and parasitic pathogens, making them both a key player in innate immunity and a potential target of infection by pathogens, including HIV. Among these PRRs is mannose receptor, a macrophage-specific protein that binds oligosaccharides, restricts HIV replication, and is downregulated by the HIV accessory protein Vpr. Vpr significantly enhances infection in vivo, but the mechanism by which this occurs is controversial. It is well established that Vpr alters the expression of numerous host proteins by using its co-factor DCAF1, a component of the DCAF1–DDB1–CUL4 ubiquitin ligase complex. The host proteins targeted by Vpr and their role in viral replication are described in detail. We also discuss the structure and function of the viral protein Env, which is stabilized by Vpr in macrophages. Overall, this literature review provides an updated understanding of the contributions of macrophages and Vpr to HIV pathogenesis.
Highlights
Phagocytosis can be mediated by a wide variety of receptors on the plasma membrane, including pattern-recognition receptors (PRRs), which directly bind pathogen-associated molecular patterns (PAMPs); complement receptors, which bind proteins of the complement system; and Fc receptors, which bind the constant regions of antibodies
This study demonstrated that Vpr directly interacted with SLX4 and DCAF1, which led to decreased steady state levels of MUS81 and EME1 and activation of SLX complex (SLXcom)
This study demonstrated that a mutation in Vpr (W54R) that prevents binding to UNG2 increased mutation of HIV genomes in macrophages
Summary
Human immunodeficiency virus type I (referred to as HIV throughout this review) is a lentivirus of the Retroviridea family [1]. RNA copies ofretroviruses the viral genome, of which are spliced host machinery generate import capability of HIV enables it to infect non-dividing cells and categorizes it as a specific for a single viral protein. The full-length viral RNA can be translated to produce Gag or new copies of polyproteins viral proteinsthat and are genomes, or itmost can enter latent state, in which transcription of. Vpu, and Nef. When the HIV genome is active, host transcriptional and translational machineries are induced to generate numerous viral proteins and genomes. The full-length viral RNA can be translated to produce Gag or Gag–Pol, two polyproteins that are cleaved to form most of the virus’s structural proteins, including the capsid, reverse transcriptase, and integrase. The viral accessory protein Vpr primarily enhances infection of macrophages [11,14], which is discussed in greater detail below
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